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Biomedical subjects

M J Bishop

Publications and source records attributed to M J Bishop.

At least 37 records · Page 2Linked to original sources
PubMed1997

Dexamethasone treatment does not ameliorate subglottic ischemic injury in rabbits.

BACKGROUND: Following tracheal intubation, a small proportion of patients develop laryngeal inflammation or tissue necrosis severe enough to result in clinical symptoms. Although corticosteroids are frequently advocated to prevent such injury, human studies have been inconclusive because of the low incidence of the problem. This study developed a rabbit model of endotracheal tube-induced laryngeal injury to test the hypothesis that a corticosteroid, dexamethasone, could ameliorate the inflammation and necrosis. METHODS: Subglottic injury was induced in 21 anesthetized rabbits by inflating the cuff of an endotracheal tube to 100 mm Hg with the cuff just below the vocal cords. Every 30 min for 2 h, the cuff was deflated, the tube turned 90 degrees, and the cuff then reinflated. After 2 h, the rabbits' tracheas were extubated. Rabbits were divided into two groups: the treatment group received dexamethasone (1 mg/kg) i.v. 1 h prior to extubation with the dose repeated 6 h following extubation; the untreated group received a saline solution placebo. Four additional rabbits were anesthetized for the same period but did not have a tracheal tube inserted. All rabbits were killed 24 h later and the larynxes were harvested. Sections through the larynx at the level of the cricoid cartilage were randomized and submitted blindly to a veterinary pathologist. Larynxes were scored and ranked according to the severity of mucosal inflammation and necrosis, and submucosal hemorrhage, edema, inflammation, and necrosis. Specimens were also evaluated for focal vs diffuse disease. RESULTS: Injured rabbits demonstrated focal to diffuse mucosal and submucosal inflammation and necrosis. Inflammatory exudates were present in sections from most of the injured rabbits and large sections of the larynxes were denuded of epithelium. There were no differences in injury scores between the treated and untreated rabbits. The four uninjured control rabbits had normal larynxes. CONCLUSIONS: Two hours of endotracheal tube cuff inflation to 100 mm Hg causes an inflammatory laryngeal injury. The histologic features of the injury are unaltered by treatment with 2 mg/kg dexamethasone.

Animals↗
PubMed1996

Characterization of delta opioid receptors in lung cancer using a novel nonpeptidic ligand.

Cancer cells are often characterized by the presence of membrane receptors not normally associated with nontransformed cells from the same tissue type. Recent studies have demonstrated increased expression of high-affinity binding sites for opioid receptor-selective ligands in lung cancer cell lines relative to normal lung tissue. We investigated the binding of a nonpeptidic delta opioid receptor ligand in small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC) cells with the aim of developing the ligand as a novel lung cancer imaging agent. The ligand, [3H] (+)-4-[alpha-R)-alpha-((2S,5R)-4-allyl-2,5-dimethyl-1-piperazinyl)-3- hydroxybenzyl)-N,N-diethylbenzamide ([3H](+)BW373U86), bound with high-affinity [Kd (dissociation constant) = 0.066 +/- 0.012 nM] to membranes prepared from six different SCLC cell lines but not to those from seven NSCLC cell lines, including one mesothelioma. The number of biding sites varied from 10 to 300 fmol/mg membrane protein. Competition binding studies demonstrated displacement of [3H](+)BW373U86 binding by the delta-selective antagonists naltriben and 7-benzylidenenaltrexone but not with the mu- and kappa- selective antagonists D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH2 and trans-(+/-)-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)cyclohexyl]ben zeneacetamide methanesulfonate. Mean apparent Kis for naltriben and 7-benzylidenenaltrexone in membranes from two SCLC cell lines were 0.17 and 3.9 nM, respectively, but were >10 microM for the mu and kappa ligands. The nonselective antagonist naloxone displaced [3H](+)BW373U86 binding with an apparent Ki of approximately 29 nM. On the basis of these data, we believe the lung cancer receptor to be similar, if not identical, to the human brain delta opioid receptor. The lack of high-affinity [3H](+)BW373U86 binding in normal mouse lung membranes suggests a potential role for this ligand as a novel therapeutic or imaging agent.

Animals↗
PubMed1996

Exposures to inhalable and "total" oil mist aerosol by metal machining shop workers.

Several recent studies have compared worker personal aerosol exposures as measured by the current method with those obtained by a new approach based on collecting the inhalable fraction, intended to represent all the particles that are capable of entering through the nose and/or mouth during breathing. The present study investigated this relationship for a metal machining facility where aerosols were generated from severely refined, nonaqueous ("straight") cutting oils used during the lathe working of metal rod stock. Workers (n = 23) wore two personal aerosol samplers simulataneously, one of the 37-mm type (for "total" aerosol exposure, E37) and the other of the Institute of Occupational Medicine (IOM) type (for inhalable aerosol exposure, EIOM). The data were analyzed by weighted least squares linear regression to determine the coefficient S in the relation EIOM = S.E37. It was found that S = 2.96 +/- 0.60. This ratio-in which exposure to inhalable aerosol was greater than to "total" aerosol-is consistent with previous observations in other industries. The relative coarsenss of the oil mist aerosol, as estimated by cascade impactor measurements, probably explains the difference between the sampling methods. The collection of large "splash" droplets, may also contribute. Future occupational aerosol standards for metalworking fluids will be based on the new, health-related criteria, and exposures will be assessed on the basis of the inhalable fraction. Results of studies like that described here will enable assessment of the impact on future workplace aerosol exposure assessments of introducing new standards.

Aerosols↗
PubMed1996

Comparative effects of thiopentone and propofol on respiratory resistance after tracheal intubation.

To compare the effects of propofol and thiopentone on tracheal intubation-induced bronchoconstriction, 37 patients were allocated randomly to anaesthesia with either thiopentone 4 mg kg-1 followed by a 15-mg kg-1 h-1 continuous infusion or propofol 3 mg kg-1 followed by a 9-mg kg-1 h-1 continuous infusion. Intubation was facilitated by vecuronium 0.1-0.2 mg kg-1. Respiratory system resistance (Rrs) was measured by a CP-100 pulmonary function monitor, 5 min after intubation. The 5-min post-intubation Rrs values were significantly lower in the propofol group (8.5 (SD 1.5) cm H2O litre-1 S-1) than in the thiopentone group (10.9 (3.2) cm H2O litre-1 S-1). Thirty minutes after commencing isoflurane-nitrous oxide anaesthesia, Rrs declined by 17.5 (SEM 3.6)% from baseline in the thiopentone group, but by only 1.6 (2.6)% in the propofol group. We conclude that the dose of propofol administered provided more protection against tracheal intubation-induced bronchoconstriction than an induction dose of thiopentone.

Adult↗
PubMed1996

Isoflurane anesthesia does not add to the bronchodilating effect of a beta 2-adrenergic agonist after tracheal intubation.

This double-blind study investigates whether isoflurane/N2O anesthesia adds to the bronchodilating effect of the beta 2-adrenergic agonist, fenoterol, after an endotracheal tube (ETT)-induced increase in airway resistance. Forty-five patients with ASA physical status I-II were randomly assigned to two groups: fenoterol-treated patients (n = 23) were given three metered-dose inhaler puffs (600 micrograms) of fenoterol 10 min before induction of anesthesia and placebo-treated patients (n = 22) received three puffs of an aerosol containing no medication. Anesthesia was induced with thiopental and vecuronium intravenously. Respiratory system resistance (Rrs) was measured using a CP-100 pulmonary function monitor 5 min after endotracheal intubation. Inhalation anesthesia was then begun using 50% N2O in O2 with end-tidal 1.3% isoflurane. Rrs measurements were repeated at 5, 15, and 30 min after the initiation of inhalation anesthesia. Postintubation Rrs was significantly lower in the fenoterol-treated patients than in the placebo-treated patients. Rrs declined by a mean of 17.1% after 30 min of inhalation anesthesia in the placebo-treated patients but declined by only 1.4% in the fenoterol-treated patients (P < 0.05 for fenoterol provides protection versus placebo). Our results confirm that fenoterol provides protection against ETT-induced increase of airway resistance. However, isoflurane, while a potent bronchodilator, does not add to the effect of fenoterol.

Adrenergic beta-Agonists↗
PubMed1996

Comparison of the effects of etomidate, propofol, and thiopental on respiratory resistance after tracheal intubation.

BACKGROUND: Tracheal intubation frequently results in reversible bronchoconstriction. Propofol has been reported to minimize this response in healthy patients and in asthma patients, but may be unsuitable for hemodynamically unstable patients for whom etomidate may be preferable. The current study examined respiratory resistance after tracheal intubation after induction with either thiopental, etomidate, or propofol. A supratherapeutic dose of etomidate was used to test the hypothesis that the bronchoconstrictive response could be minimized by deep intravenous anesthesia. METHODS: Seventy-seven studies were conducted in 75 patients. Anesthesia was induced with either 2.5 mg/kg propofol, 0.4 mg/kg etomidate, or 5 mg/kg thiopental. Respiratory resistance was measured at 2 min after induction. RESULTS: Respiratory resistance at 2 min was 8.1 +/- 3.4 cmH2O.1(-1).s (mean +/- SD) for patients receiving propofol versus 11.3 +/- 5.3 for patients receiving etomidate and 12.3 +/- 7.9 for patients receiving thiopental (P < or = 0.05 for propofol vs. either etomidate or thiopental). CONCLUSIONS: Respiratory resistance after tracheal intubation is lower after induction with propofol than after induction with thiopental or after induction with high-dose etomidate.

Adult↗
PubMed1996

Pressures required to move gas through the native airway in the presence of a fenestrated vs a nonfenestrated tracheostomy tube.

SUBJECT: It is occasionally desirable for patients with a tracheostomy tube to breathe through their native airway. We hypothesized that capped tracheostomy tubes with cuffs deflated would create substantial additional resistance to airflow without fenestration but would provide minimal resistance to airflow when the tube had a fenestration. METHODS: Two tracheal models were tested simulating a large (26 mm) and an average (18 mm) trachea. Tests were carried out with fenestrated and nonfenestrated tracheostomy tubes of sizes ranging from No. 4 to No. 10. Negative pressure inspiration was simulated using suction. RESULTS: With a large trachea or small tubes, the suction required to generate flows of 40 L/min or greater remained less than 5 cm H2O with or without a fenestration. However, with an average-sized trachea and no fenestration, the pressure required to generate flows of 40 L/min or greater exceeded 5 cm H2O and with No. 8 or No. 10 tubes exceeded 20 cm H2O. A fenestration routinely reduced the required pressure to less than 5 cm H2O. CONCLUSION: The effort required to move gas across the native airway in the absence of a fenestration may be substantial. If a patient is to breathe through a native airway, a fenestrated tube should be used unless the tracheostomy tube is a No. 4.

Equipment Design↗
PubMed1995

CD18-independent mechanism of neutrophil emigration in the rabbit lung after ischemia-reperfusion.

BACKGROUND: Reperfusion of ischemic lung causes an inflammatory pulmonary vascular injury characterized by increased vascular permeability and migration of inflammatory cells into the alveoli. Migration of neutrophils into the alveolus during reperfusion after 24 hours of unilateral pulmonary artery occlusion has been shown to be in part dependent on the CD18 adhesion molecule on the cell surface. The current study investigated whether reperfusion lung injury after a 1-hour period of complete lung ischemia was CD18 dependent. METHODS: Eighteen rabbits were assigned to one of three groups. Groups 1 and 2 were subjected to one hour of in situ right hilar occlusion followed by 2 hours of reperfusion. Group 3 was subjected to identical surgical dissection but the right hilum was never occluded. Group 1 rabbits received saline solution (1 mL/kg) before hilar occlusion and group 2 rabbits, monoclonal antibody 60.3, a blocking antibody for the CD18 adhesion molecule on the neutrophil surface (2 mg/kg). In 3 of the antibody-treated rabbits, flow cytometry was performed on blood neutrophils before and after administration of the antibody and 120 minutes after reperfusion. RESULTS: The rabbits in groups 1 and 2 had significantly increased alveolar neutrophil infiltrate and increased pulmonary vascular resistance compared with the rabbits in group 3. However, there was no significant difference between group 1 (saline solution treated) and group 2 (antibody treated). Antibody treatment did not block migration of neutrophils into the alveoli. Flow cytometry of circulating neutrophils demonstrated that CD18 was upregulated after reperfusion and that CD18 was fully blocked after antibody treatment for the duration of the study. CONCLUSIONS: We conclude that a 1-hour period of warm ischemia followed by reperfusion results in upregulation of CD18 but that emigration of the neutrophils into the alveoli is not CD18 dependent in this injury.

Animals↗
PubMed1995

Jet ventilation using fiberoptic bronchoscopes.

A fiberoptic bronchoscope is used to facilitate tracheal intubation in cases of difficult direct laryngoscopy. Occasionally, difficulty is encountered in advancing the endotracheal tube after the fiberoptic bronchoscope has been introduced into the trachea. This study tested the feasibility of providing jet ventilation through the suction channel of the fiberoptic bronchoscope as an interim measure under those or similar circumstances. Three commercial models of fiberoptic bronchoscopes with suction channels of 1.2-, 1.5-, and 2-mm diameter, respectively, were tested in a mechanical test lung at varying compliances and resistances using a jet injector connected to an oxygen source at 50 psi. The fiberoptic bronchoscope with the 2-mm suction channel was also studied in seven adult patients who were anesthetized and paralyzed. Jet ventilation was manually performed at the rate of 12/min for 10 min. In the mechanical test lung, the tidal volumes with 1.2-, 1.5-, and 2-mm suction channels were as follows: 280 mL, 490 mL, and 880 mL, respectively, at a compliance of 50 mL/cm H2O and normal resistance; 260 mL, 470 mL, and 820 mL, respectively, at a compliance of 50 mL/cm H2O and high resistance to simulate bronchospasm; 130 mL, 270 mL, and 890 mL, respectively, at a compliance of 20 mL/cm H2O and normal resistance; 120 mL, 220 mL, and 810 mL, respectively, at a compliance of 20 mL/cm H2O and high resistance. In anesthetized, paralyzed patients, oxygen saturation was 96% or more throughout the study.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Effect of anemia on intrapulmonary shunt during atelectasis in rabbits.

To elucidate the effects of anemia on intrapulmonary shunt, we studied a model of left lung atelectasis in anesthetized rabbits. In 10 rabbits, isovolemic anemia was produced by sequential hemodilution. Seven control rabbits were followed over time, without hemodilution. Intrapulmonary shunt (Qs/QT) was measured by using blood gas analysis and by quantitation of the percentage of blood flow to the collapsed left lung (QLl/QT) using fluorescent microspheres. In control rabbits, Qs/QT and QLl/QT decreased over time, whereas arterial PO2 increased. In hemodiluted rabbits, there was a trend toward increased Qs/QT and QLl/QT. There were significant differences in the behavior of Qs/QT, QLl/QT, and arterial PO2 between control and hemodiluted rabbits. Hemodynamic parameters, including cardiac output and pulmonary artery pressure, were not different between groups. In a third group of rabbits with pharmacologically induced acidosis but no hemodilution, Qs/QT and QLl/QT decreased over time, and arterial PO2 increased. We conclude that acute isovolemic anemia has a deleterious effect on pulmonary gas exchange, possibly through attenuation of hypoxic pulmonary vasoconstriction.

Anemia↗
PubMed1995

Practice guidelines for airway care during resuscitation.

Existing guidelines for equipment and personnel have been described. In addition, the ASA guidelines on management of the difficult airway have been presented as an example of the type of algorithm that might be used for management of the difficult airway. Whereas guidelines are not standards, it is important to recognize that as guidelines are adopted by more and more practitioners, they become "standards of care" to which we are all held accountable.

Airway Obstruction↗
PubMed1995

Evaluation and management of the difficult airway.

Even routine airway management requires specific skills that are best acquired in a controlled setting, before "trial by fire" in an emergency situation. Furthermore, recognition of a potential difficult airway and appropriate preparation prior to initiating airway intervention are critical steps in avoiding airway catastrophes in the intensive care or emergency setting. Familiarity with a difficult airway algorithm and various alternate techniques for endotracheal intubation is a mandatory requirement for all practitioners involved in airway management, and should be incorporated in critical care curricula. Critically ill patients, by nature, are at risk for complications during manipulation of the airway, and may have a higher incidence of adverse reactions to anesthesia-inducing drugs and muscle relaxants. In general, "less is more" in the intensive care unit, and techniques that preserve spontaneous ventilation during airway interventions are desirable, particularly in patients with anticipated difficult airways. All intubating sites should have a portable storage unit for equipment for managing difficult airways readily available. Correct ETT placement always should be verified by detection of exhaled CO2, and by chest radiography if prolonged intubation is planned.

Airway Obstruction↗
PubMed1994

Pulmonary artery occlusion and lung collapse depletes rabbit lung adenosine triphosphate.

BACKGROUND: Although the bronchial circulation has traditionally been thought to provide adequate blood flow for the lung when the pulmonary artery is obstructed, recent studies have demonstrated that pulmonary artery occlusion results in lung injury. We hypothesized that after pulmonary artery occlusion, aerobic lung metabolic function is altered. We studied the changes in the concentration of adenine nucleotides as markers of injury in the intact rabbit lung after pulmonary artery occlusion in the presence and absence of pneumothorax. METHODS: A thoracotomy was performed on the rabbits, and on occlusive microvascular clamp was placed on the left pulmonary artery. The rabbit lungs were studied after 24 h of in vivo left pulmonary artery occlusion (n = 5), 24 h of left pulmonary artery occlusion with the lung collapsed by pneumothorax (n = 6), or 24 h of lung collapse alone (n = 5). RESULTS: Adenosine triphosphate concentrations of the occluded left lung decreased dramatically at 24 h in the group with pulmonary artery occlusion and collapse (adenosine triphosphate concentration 196 +/- 32 ng/g for the left lung and 1,479 +/- 197 ng/g for the right lung; P < 0.001). There were no differences between the lungs in the rabbits undergoing occlusion alone or collapse alone. CONCLUSIONS: After pulmonary artery occlusion or lung collapse, adenine nucleotides are preserved if ventilation is continued. The increased permeability of rabbit lungs after 24 h of left pulmonary artery occlusion alone cannot be explained on the basis of depletion of high-energy phosphates. In the absence of ventilation due to lung collapse, pulmonary artery occlusion results in decreased adenosine triphosphate concentrations, demonstrating that the residual circulations (bronchial and pulmonary venous flow) are inadequate to support normal lung aerobic metabolism.

Adenosine Triphosphate↗
PubMed1994

Effect of prophylactic bronchodilator treatment on lung resistance after tracheal intubation.

BACKGROUND: After induction of anesthesia, lung resistance increases. We hypothesized that prophylactic bronchodilator treatment before tracheal intubation would result in a lower lung resistance after placement of the endotracheal tube. METHODS: Forty-two adult patients were randomized to receive one of three inhaled medications 1 h before surgery. All patients first underwent pulmonary function tests. Patients then received either inhaled albuterol (360 micrograms) (n = 12), inhaled ipratropium bromide (72 micrograms) (n = 15) or a placebo inhalation (n = 15). Two, 5, and 15 min after tracheal intubation, lung resistance was measured using the method of von Neergard and Wirtz. RESULTS: Patients who received either bronchodilator had significantly lower lung resistance after intubation than those receiving placebo. At 2 min, lung resistances were 12.7 +/- 1.4 cmH2O.l-1.s-1 (mean +/- SEM) for the placebo group, 6.4 +/- 3.1 cmH2O.l-1.s-1 for the ipratropium-treated group (P < 0.05 vs. placebo), and 7.2 +/- 0.8 cmH2O.l-1.s-1 for the albuterol-treated group (P < 0.05 vs. placebo). The differences in lung resistance persisted through the final measurement at 15 min. Three of fifteen placebo-treated patients developed audible wheezing whereas no patients developed wheezing in either bronchodilator-treated group (P < 0.05 by Fisher's exact test). Although smokers and nonsmokers in the placebo group developed similar resistances after intubation, bronchodilator treatment resulted in lower resistance in nonsmokers than in smokers (P < 0.05). CONCLUSIONS: Prophylactic treatment with either an inhaled beta 2-adrenergic agonist or an inhaled cholinergic antagonist produced lower lung resistance after intubation when compared with an inhaled placebo medication. The effect was more pronounced in nonsmokers than in smokers.

Administration, Inhalation↗